U.S. NAVAL Flight Surgeon’s Manual - Operational Medicine · 2016-07-07 · U.S. NAVAL Flight Surgeon’s Manual THIRD EDITION 1991 Prepared by NAVAL AEROSPACE MEDICAL INSTITUTE

U.S. NAVAL

Flight Surgeon’s Manual

THIRD EDITION

1991

Prepared by

NAVAL AEROSPACE MEDICAL INSTITUTE

Under the auspices of

THE BUREAU OF MEDICINE AND SURGERYDepartment of the Navy

For sale by the Superintendent of Documents, U.S. Government Office, Washington, D.C. 20402

Project direction by

Editorial BoardNaval Aerospace Medical Institute

Captain Ronald K. Ohslund, MC, USNCaptain Conrad I. Dalton, MC, USN

Commander Gary G. Reams, MC, USNCommander Jerry W. Rose, MC, USN

Lieutenant Commander Richard E. Oswald, MC, USN

Project ManagersCommander Jerry W. Rose, MC, USN

Lieutenant Commander Richard E. Oswald, MC, USN

ii

FOREWORD

As we quickly approach the 21st Century, the Navy Medical Department stands ready to take

on some of the greatest challenges it has ever faced. With the Cold War now a part of history, wemust learn to operate within a new world order; one in which we must maintain our level ofreadiness within the context of an ever changing geopolitical environment. Critical to our futuresuccess in responding to the needs of the Fleet and Fleet Marine Force will be our ability to

synthesize past experiences into our current knowledge base while simultaneously projectingrequirements into the future. One important way of accomplishing such a task is by the sharing ofinformation as quickly and efficiently as possible. The Third Edition of the Flight Surgeon’s

Manual represents a major tool in this process. It is the culmination of 13 years of effort indistilling out the very best of aerospace science and technology.

We have entered a new era on the battlefield. Technology has made it possible for aircraft to

out perform their occupants. Innovation has given us a glass cockpit whose avionics suite can

easily overload the aviator not aided by multiple high speed computers. Weaponry has made itpossible to inflict devastating physiologic damage without killing an aircraft’s occupants ordamaging the airframe. And we are poised on the verge of hypersonic mass transit. Each of thesephenomena could not be understood or countered if it were not for the efforts of the AerospaceMedicine Team.

The Third Edition is dedicated to the pioneering spirit of those in operational medicine whose

interests have kept our country strong and our course true to the cutting edge of technology. Forit is only through the noteworthy efforts of all members of the Aerospace Medicine Communityover the last several decades that we continue to carry on our proud tradition of quality medicalsupport of the Fleet.

James A. Zimble

Vice Admiral, Medical Corps

United States NavyDirector of Naval Medicine/

Surgeon General

iii

PREFACE

The unique aspect of aerospace medicine as practiced by a U.S. Naval Flight Surgeon is the re-quirement to function independently at isolated duty stations. Whether at sea, on a small patch of

land in mid-ocean, or at expeditionary airfield of the Fleet Marine Force, Flight Surgeons areoften called upon to make medical and administrative decisions which affect the lives and careers

of the most critical assets in the naval service - members of the Naval Aviation community. Not

only must we treat the day to day medical problems but we must be prepared to deal with a vastarray of casualties which all too frequently remind us of the danger inherent in Naval Aviation.

This manual is both an introduction to the various aspects of Naval Aerospace Medicine and aguide for dealing with the other complex administrative procedures known as “the system.” This

revision has evolved from questions most frequently asked, errors most commonly made, with a

dash of seasoned advice passed down to the youngsters. The manual should stand between the

Manual of the Medical Department and a current text on aerospace medicine. It is written to pro-vide the Flight Surgeon with a reminder of the material presented in the formal course ofaerospace medicine and as a reinforcement of the fact that the U.S. Naval Flight Surgeon standsat the apex of military operational medicine.

The U.S. Naval Flight Surgeon’s Manual was originally designed to be updated at frequent in-

tervals. This revision is the first since 1977 and has therefore resulted in an extensive rewrite of

most of the chapters. The plan is to keep the manual current through annual submissions of newmaterial by the Naval Aerospace Medical Institute and through contributions from the users ofthis text.

R.K. Ohslund

Captain, MC, USNCommanding Officer

Naval Aerospace Medical Institute

v

ACKNOWLEDGMENTS

The Third Edition of the U.S. Naval Flight Surgeon’s Manual is the result of a team productionwith each member performing his required task. No one individual or select group of individuals

was responsible. Some chapters are updates of the second edition; others have been completelyrewritten.

The multiple tasks necessary for the publication of this manual were accomplished in addition

to the normal duties of each contributor. Special recognition should be made of the contributingauthors. They are:

Authors, Second Edition

LCDR Joseph M. Andrus, MC, USNCDR Don S. Angelo, MC USNCDR C.H. Bercier, MC, USNCAPT O.G. Blackwell, MC, USN

CDR W.A. Buckendorf, MC, USN

CAPT. Eugene J. Colangelo, MC, USN

Ms. Jacque DevineCAPT Frank E. Dully, Jr., MC, USN

CAPT F.S. Evans, MC, USNMartin G. Every, MSCAPT J.E. Felder, MC, USN

CDR Donald E. Furry, MSC, USN

LT James A. Gessler, MC, USN

Mr. James W. GreeneFrederick E. Guedry, Jr., Ph.D.

LT David T. Hargraves, MSC, USNCDR Norman G. Hoger, MC, USNCDR Gary L. Holtzman, MC, USN

CDR William M. Houk, MC, USNCAPT Joseph Kerwin, MC, USN

CDR T.F. Levandowski, MSC, USN

LCDR Neil R. McIntyre, MC, USNR

vii

U.S. Naval Flight Surgeon’s Manual

CDR C.J. McAllister, MC, USNCDR Richard A. Millington, MC, USNCAPT J.D. Morgan, MC, USNLCDR L.P. Newman, MC, USNRCAPT P.F. O’Connell, MC, USNRJames F. Parker, Jr., Ph.D.CAPT Joseph A. Pursch, MC, USNRonald M. Robertson, Ph.D.CAPT. E.J. Sacks, MC, USNCAPT Richard J. Seeley, MC, USNCDR Phillip W. Shoemaker, DC, USNLCDR Felix Zwiebel, MC, USN

Authors, Third Editon

CDR Michael R. Ambrose, MC, USNCAPT James C. Baggett, MC, USNAnnette G. Baisden, MACDR Robert Bason, MSC, USNCAPT Charles H. Bercier, Jr., MC, USNCAPT S. William Berg, MC, USNCDR Bruce K. Bohnker, MC, USNCAPT Philip T. Briska, MC, USNCDR Jonathan B. Clark, MC, USNCDR D.E. Deakins, MC, USNChuck E. DeJohn, D.O.LCDR Michael Dubik, MC, USNLCDR William B. Ferrara, MC, USNCDR James R. Fraser, MC, USNFederick C. Guill, B.S.M.E., M.S.LCDR Gerald B. Hayes, MC, USNRLCDR F.D. Holcombe, MSC, USNRCAPT Gary L. Holtzman, MC, USNCAPT Robert E. Hughes, MC, USNCDR Wesley S. Hunt, MC, USNLCDR William L. Little, MSC, USNLCDR Steven G. Matthews, MSC, USNCAPT Andrew Markovitz, MC, USNR

viii


LCDR Michael H. Mittelman, MSC, USN

CDR Carroll J. Nickle, MC, USNCDR Richard G. Osborne, MC, USNLCDR Richard E. Oswald, MC, USNCDR Jerry W. Rose, MC, USN

CAPT E.J. Sacks, MC, USN

The essential logistic, clerical, and secretarial support which was vital to the successful comple-

tion of this project was carried out by:

Support Personnel

Word Processing

Karen Strickland Brewton

Sue BondurantRose Ann Spitzer

Computer AssistantsCDR Bruce K. Bohnker, MC, USNMichelle Marshall

Technical Publications Editor/WriterMary M. Harbeson

Technical Manuals Writer (Aircraft)Claudia J. Lee

Technical Illustrations

Robert Lewis Scott

Fiscal OfficersLT Danny D. Urban, MSC, USNRLTJG Roland E. Arellano, MSC, USN

Facilities Management

HMl Richard D. Wilson

ix

TABLE OF CONTENTS

PageChapter 1

Physiology of Flight . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1-1

Chapter 2

Acceleration and Vibration . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2-l

Chapter 3

Vestibular Function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3-1

Chapter 4Space Flight Considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4-l

Chapter 5

Internal Medicine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5-l

Chapter 6Psychiatry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6-l

Chapter 7Neurology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7-l

Chapter 8Otorhinolaryngology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8-1

Chapter 9

Ophtalmology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9-l

Chapter 10Dermatology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10-l

Chapter 11

Sexually Transmitted Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11-1

Chapter 12

Aerospace Psychological Qualifications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12-l

Chapter 13Aviation Medicine with Fleet Marine Forces . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13-l

xi


Chapter 14The Aircraft Carrier . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14-l

Chapter 15Disposition of Problem cases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15-1

Chapter 17

Medication and Flight . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17-l

Chapter 18Alcohol Abuse and Alcoholism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18-1

Chapter 19Fatigue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19-1

Chapter 20Thermal Stresses and Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20-l

Chapter 21

Toxicology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21-1

Emergency Escape from Aircraft . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22-1Chapter 22

Chapter 23Aircraft Mishap Investigations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23-l

Chapter 24

Aircraft Accident Survivability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24-l

Chapter 25Aircraft Accident Autopsies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25-l

Historical Chronology of Aerospace Medicine in the U.S. Navy . . . . . . . . . . . . . . . . . . . . . . . A-l

Chapter 16Aeromedical Evacuation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16-l

Appendix A

xii

CHAPTER 1

PHYSIOLOGY OF FLIGHT

The AtmosphereRespiratory PhysiologyHypoxiaHyperventilationPositive Pressure BreathingCabin Pressurization

Rapid DecompressionTrapped Gas

Bubble Related Diseases

Oxygen ToxicityOxygen EquipmentReferences and Bibliography

The Atmosphere

The atmosphere of the Earth can be thought of as an ocean of gases which extend from the

Earth’s surface to space and is composed primarily of nitrogen, oxygen, argon and trace gases.The specific composition of the dry atmosphere is presented in Table l-l. These fractional con-centrations remain relatively constant to the outer limits of the atmosphere. Just as a column ofwater exerts a force or weight per unit area, the column of air above a specific point exerts apressure (force), which usually is expressed in millimeters of mercury. Table 1-2 presents many ofthe units of pressure measurement in common use. This table includes both altitude measures and

sea water depth measures. The relationship of pressure and temperature changes produced by theforce of the column of air is presented in Table 1-3, from sea level to 100,000 feet, in both Englishand metric equivalents.

l - l


The atmosphere can be divided into several different concentric, spherical divisions based upon

physical and chemical properties. DeHart (1985) and Campen (1960) identify principle

characteristics of each of the atmospheric layers as illustrated in Figures 1-1, and described inTable l-4.

Table l-l

Composition of the Dry Atmosphere at Sea Level

G a s Frac t ionsVolume

(% by volume)

Nit rogen 78.03

Oxygen 20.95

A r g o n 0.93

C a r b o n d i o x i d e 0.03

N e o n 1.82 x 10-3

H e l i u m 5.24 x 10-4

Kryp ton 1.14 x 10-4

H y d r o g e n 5.00 x 10-5

X e n o n 8.70 x 10-6

l-2

Physiology of Flight

Table 1-2

Equivalent Pressures, Altitudes and Depths

(Billings, 1973b).

1-3


Table l-3

Altitude-Pressure-Temperature Relationships Based on the U.S. Standard Atmosphere

Altitude Pressure Temperature

1-4


Table l-3 (Continued)

Altitude-Pressure-Temperature Relationships Based on the U.S. Standard Atmosphere

Altitude Pressure Temperature

l-5


Figure l-l. Identification of atmospheric shells (Ware, in DeHart, 1985).

l-6


Table 1-4

Description of Atmospheric Shells

Name

Troposphere

Stratosphere

Mesosphere

Thermosphere

Heterosphere

Temperature

Description

The region nearest the surface, which has a more or less uniform degree of temperature withaltitude. The nominal rate of temperature decrease is 6.5 °K/km, but inversions are common.The troposphere, the domain of weather, is in convective equilibrium with the sun-warmedsurface of the earth. The tropopause, which occurs at altitudes between 6 and 19 km (higherand colder over the equator), is the domain of high winds and highest cirrus clouds.The region next above the troposphere, which has a nominally constant temperature. Thestratosphere is thicker over the poles and thinner, or even nonexistent, over the equator. Themaximum of atmospheric ozone is found near the stratopause. Rare nacreous clouds are alsofound near the stratopause. The stratopause is about 25 km altitude in middle latitudes.Stratospheric temperatures are in the order of arctic winter temperatures.The region of the first temperature maximum. The mesosphere lies above the stratosphere andbelow the major temperature minimum, which is found near 80 km altitude and constitutesthe mesopause. This is a relatively warm region between two cold regions, and the regionwhere most meteors disappear. The mesopause is found at altitudes of from 70 to 85 km. Themesosphere is in radiative equilibrium between ultraviolet ozone heating by the upper fringeof the ozone region and the infrared ozone and carbon dioxide cooling by radiation to space.The region of rising temperature above the major temperature minimum around the altitudeof 80 km. There is no upper altitude limit. This is the domain of the auroras. Temperaturerises at the base of the thermosphere are attributed to too infrequent collisions amongmolecules to maintain thermodynamic equilibrium. The potentially enormous infraredradiative cooling by carbon dioxide is not actually realized owing to inadequate collisions.

Composition

Homosphere The region of substantially uniform composition, in the sense of constant mean molecularweight from the surface upward. The composition changes here primarily because of thedissociation of oxygen. Mean molecular weight decreases accordingly. The ozonosphere, hav-ing its peak concentration near the stratopause altitude, does not change the mean molecularweight of the atmosphere significantly.The region of significantly varying composition above the homosphere and extending in-definitely outward. The “molecular weight” of air diminishes from 29 at about 90 km to 16at about 500 km. Well above the level of oxygen dissociation, nitrogen begins to dissociate,and diffusive separation (lighter atoms and molecules rising to the top) sets in.

Chemical Reactions

Chemosphere The region where chemical activity (primarily photochemical) is predominant. Thechemosphere is found within the altitude limits of about 20 to 110 km.

Ionization

Ionosphere The region of sufficiently large electron density to affect radio communication. However, on-ly about one molecule in l000 in the F2 region to one molecule in 100,000,000 in the D region isionized. The bottom of the ionosphere, the D region, is found at about 80 km during the day. At nightthe D region disappears, and the bottom of the ionosphere rises to 100 km. The top of the ionosphere isnot well defined but has often been taken to be about 400 km. The upper limit has recently been extend-ed upward to 100 km based on satellite and rocket data.

(DeHart , 1985)

1-7


Ozone (03) is produced in the upper atmosphere by the sun’s radiation. Ozone is a highly toxicgas which significantly impacts respiratory functions. Significant concentrations are found be-

tween 40,000 and 140,000 feet as illustrated in Figure l-2. This concentration of ozone is impor-tant in that it absorbs the majority of radiation in the ultraviolet range (wave lengths shorter than2900 angstrom units), thereby screening potentially harmful radiation most often associated with

skin cancer.

Figure 1-2. Relationship between temperature, altitude, and atmospheric zones.

1-8


The characteristics and divisions of the atmosphere describe the physical features of the at-mosphere. In the field of aerospace medicine it is man’s physiological response to the environ-ment which is of primary concern. Based on man’s physiological responses, the atmosphere can

be divided into three zones: the physiological zone, the physiologically deficient zone, and thespace equivalent zone.

Physiological Zone

This zone extends from sea level to 10,000 feet. It is the zone to which man’s body is well

adapted. The oxygen level within this zone is sufficient to keep a normal, healthy individual

physiologically fit without the aid of special protective equipment. The changes in pressure en-countered with rapid ascents or descents within this zone can produce ear or sinus trapped gasproblems; however, these are relatively minor when compared to the physiological impairmentsencountered at higher altitudes.

Physiologically Deficient Zone

This zone extends from 10,000 feet to 50,000 feet. Noticeable physiological deficits begin to oc-cur above 10,000 feet. The decreased barometric pressure in this zone results in a sufficient ox-ygen deficiency to cause hypoxic hypoxia. Additional problems may also arise from trapped andevolved gases. Protective oxygen equipment is necessary in this zone.

Space Equivalent Zone

From a physiological viewpoint space begins when 50,000 feet is reached since supplemental100 percent oxygen no longer protects man from hypoxia. The means of protecting an individualat 50,000 feet or above, are such that they will also protect him in true space (i.e., pressure suitsand sealed cabins). The only additional physiological problems occurring within this zone, whichextends from 50,000 feet to 120 miles, are possible radiation effects and the boiling of body fluids(ebullism) in an unprotected individual. Boiling of body fluids will occur when the total

barometric pressure is less than the vapor pressure of water at 37° C [47 millimeters of mercury

(mm Hg)] which is reached at an altitude of 63,500 feet (Armstrong’s Line).

Respiratory Physiology

Gas physiology is one of the cornerstones of aviation medicine. A great deal of work has been

done in this field in connection with high-altitude military and civilian aircraft development as

well as in support of manned space flight. The purpose of this chapter is not to present a compen-

1-9


dium of this information but rather a skeleton upon which an interested flight surgeon may buildthrough additional reading.

The four principal gases of interest in aviation medicine are oxygen, nitrogen, carbon dioxide,

and water vapor.

The principal functions of respiration are to transport alveolar oxygen to the tissues and totransport tissue carbon dioxide back to the lungs. The process is effected by transporting gases

through the upper respiratory tract and trachea to the alveoli, letting the gases of alveoli andpulmonary capillary blood reach equilibrium with each other, transporting the arterial blood totissue, where tissue gases reach equilibrium with arterial gases in the capillaries, and returning the

blood to the lungs to repeat the process.

Individual cells within the tissues of the body are basically fluid in composition and, as such,are essentially incompressible. Pressure applied uniformly to a tissue surface thus is readilytransmitted throughout the tissue and to adjoining structures. Changes in the pressure environ-ment do not produce cellular distortion but instead simply change the pressure of gases contained

within the body. The manner in which changes in gas pressure affect the body can be expressed in

terms of the classic laws of gas mechanics.

Classic Laws of Gas Mechanics

Boyle’s Law. Boyle’s Law states that the volume of a gas is inversely proportional to itspressure, temperature remaining constant. This means that at 18,000 feet, where the pressure is

approximately half that of sea level, a given volume of gas will attempt to expand to twice its in-

itial volume in order to achieve equilibrium with the surrounding pressure.

Charles’ Law. Charles’ Law states that the pressure of a gas is directly proportional to its ab-

solute temperature, volume remaining constant. The contraction of gas due to temperaturechange at altitude, however, in no manner compensates for the expansion due to the correspon-ding decrease in pressure.

Dalton’s Law. Dalton’s Law of partial pressures states that each gas in a mixture of gases

behaves as if it alone occupied the total volume and exerts a pressure, its partial pressure, in-

dependent of the other gases present. The sum of the partial pressures of individual gases is equalto the total pressure. Using this law, one can calculate the partial pressure of a gas in a mixturesimply by knowing the percentage of concentration in that mixture.

l-10


Henry’s Law. Henry’s Law states that the amount of gas in a solution varies directly with thepartial pressure of that gas over the solution.

Graham’s Law. Graham’s Law states that the relative rates of diffusion of gases under the

same conditions of temperature and pressure are inversely proportional to the square roots of thedensities of those gases. Gases with smaller molecular weights will diffuse more rapidly..

Pulmonary Ventilation

Ventilation is a cyclic process by which fresh air or a gas mixture enters the lungs and

pulmonary air is expelled. The inspired volume is greater than the expired volume because the

volume of oxygen absorbed by the blood is greater than the volume of carbon dioxide, which isreleased from the blood. Since gas exchange occurs solely in the alveoli and not in the conducting

airways, the estimation of alveolar ventilation rate (i.e., the amount of gas which enters thealveoli per minute) is the most important single variable of ventilation.

Pulmonary ventilation does not occur evenly throughout the alveoli since normal lungs do notbehave like perfect mixing chambers, nor is the pulmonary capillary network evenly distributed

throughout the lungs. Ventilation, therefore, must be readjusted regionally to match the in-

creased or decreased blood flow, or some of the alveoli will be relatively under or over ventilated.

The even distribution of pulmonary capillary blood flow is as important as an even distribution ofinspired air to the alveoli for normal oxygenation of the blood.

Gaseous Diffusion

Respiratory gas exchange in the lungs is accomplished entirely by the process of simple diffu-

sion. The direction and amount of movement of the molecules depend upon the difference in par-tial pressure on both sides of the alveolar membrane. Normally, molecular oxygen moves from aregion of higher partial pressure to one of lower partial pressure. The volume of gas which canpass across the alveolar membrane per unit time at a given pressure is the diffusing capacity of thelungs.

The diffusing capacity is not only dependent on the difference in partial pressure of the gas in

the alveolar air and pulmonary capillary blood, but it is also proportional to such factors as the

effective surface area of the pulmonary vascular bed. It is inversely proportional to the average

thickness of the alveolar membrane and directly proportional to the solubility of the gas in themembrane. The normal values for diffusing capacity range from 20 to 30 ml 02/min/mm Hg fornormal young adults.

l-11


Pulmonary Capillary Blood Flow

Pulmonary capillary blood flow must be adequate in volume and well distributed to all of theventilated alveoli to insure proper gas exchange. Underperfused or poorly ventilated alveoli canbecome a serious matter during flight when G forces acting on the body result in a redistributionof pulmonary capillary blood flow. During exposure to positive (+ Gz) accelerative forces, the

blood flow is directed to the lung bases, whereas, during exposure to negative (- Gz) accelera-tion, the flow is toward apical areas.

Composition of Respired Air

The composition of the atmosphere is remarkably constant between sea level and an altitude of

300,000 feet. Nitrogen and oxygen are the most abundant gases in the atmosphere as shown inTable l-l. From a practical standpoint, in the study of the effects of altitude on the human body,the percent concentrations of the other gases are considered negligible and are ignored. It is con-

venient, therefore, to consider air as about four fifths (79 percent) nitrogen and one fifth (21 per-cent) oxygen.

Atmospheric Air

In the dry air at sea level, the partial pressures of the constituent gases according to Dalton’sLaw are:

P O 2 = 760 mm Hg x 0.2075 = 157.7 mm HgP N 2 = 760 mm Hg x 0.7902 = 600.6 mm HgP C 0 2 = 760 mm Hg x 0.003 = 0.2 mm Hg

Tracheal Air

When inspired air enters the respiratory passages, it rapidly becomes saturated with water

vapor and is warmed to body temperature. The water vapor has a constant pressure of 47 mm Hgat the normal body temperature of 98.6° F, regardless of the barometric pressure. Accordingly,the sum of the partial pressures of the inspired gases no longer equals the barometric pressure, but

instead equals the barometric pressure minus the water vapor pressure. Thus, the tracheal partialpressure of inspired gases can be calculated as follows:

Ptr = (PB - 47) x FI

1-12


where

Ptr = The tracheal partial pressure of the inspired gasPB = Barometric pressureFI = The fractional concentration of the inspired gas.

Aveolar Air

The theoretical alveolar (alv) PO2 for any altitude can be calculated if one knows the

barometric pressure and the dry fraction (percentage) of oxygen in the inhaled gas. A constant,sea level ventilation rate and a normal metabolic rate are presumed for the sake of simplicity.With tracheal (tr) PH2O a constant 47 mm Hg, PCO2 (alv) a constant 40 mm Hg, a barometricpressure at 10,000 feet of 523 mm Hg, and a dry fraction of oxygen of 21 percent, then at 10,000feet breathing air,

PO2(tr) = (PB - PH2O[tr]) x .21 or

PO2(tr) = .21 (523-47) = 99.96 mm Hg.

However, in the transition from tracheal gas to alveolar gas, the PO2 is reduced and PCO2 isincreased. The PN2 remains the same. Therefore,

PO2(alv) =PO2(tr) - PCO2(alv)

PO2(alv) = 9 9 . 9 6 mm H g . - 4 0 mm H g . = 6 0 mmH g .

Actual measurements of PO2(alv) at various altitudes derived from both breathing air and

breathing 100 percent oxygen are presented in Table l-5. The PO2(alv) at 10,000 feet breathing

air was measured to be 61 mm Hg. This drop in PO2 with ascent causes a gradually increasinghypoxic stimulus to respiration (via the chemoreceptors in the area of the carotid sinus) resultingin an increased respiratory exchange rate (RER) and an increased PO2(alv) over that calculated.

There also is a decreased PCO2(alv). Table 1-5 can be used for calculations when measured dataare not available.

Table l-6 shows measured changes at sea level in the partial pressure of the gases at various sitesin the respiratory cycle. This is illustrated graphically for oxygen and carbon dioxide in Figurel-3.

l-13

14.

Table 1-5

Tracheal Oxygen Pressure, Alveolar Oxygen Pressure, and Carbon Dioxide Pressure inthe Alveolar Gas When Breathing Air and 100 Percent Oxygen at Physiologically Equivalent Altitudes

Physiology of Plight

Table l-6

Partial Pressures of Respiratory Gases at Various Sites in Respiratory Circuit of Manat Rest at Sea Level

Figure 1-3. Partial pressures of O2 (above) and CO2 (below) in air at sea level and at variouspoints within the body (Billings, 1973a).

1-15


Oxygen Transport

Oxygen is carried in the blood both in simple physical solution and in loose chemical combina-

tion with hemoglobin in the form of oxyhemoglobin. The oxygen transport capacity of one gram

of hemoglobin is 1.34 ml of oxygen. Therefore, the capacity for 100 ml of blood is about 20 ml ofoxygen (presuming normal hemoglobin to be 14.7 gm/l00 ml) and represents 100 percenthemoglobin saturation. Normally, arterial hemoglobin in an individual breathing air at sea level is98 percent saturated. When breathing 100 percent oxygen at sea level pressure, the hemoglobinbecomes 100 percent saturated, and additional oxygen goes into simple solution in the plasma.The total of additional oxygen so transported is 11 percent greater than normal.

In Figure 1-4, a family of oxygen-hemoglobin dissociation curves is presented. From thesecurves it can be seen that the blood leaves the pulmonary capillary bed with the hemoglobin about98 percent saturated. Even if the PO2(alv) is reduced by 20 mm Hg, the saturation is reduced by

only three to four percent. In the tissue capillaries, however, a small decrease in oxygen tensioncauses changes in the dissociation curve which result in a large quantity of oxygen being madeavailable to the tissues. The upper section of the dissociation curves (Figure 1-4A) remains

relatively flat through an oxygen tension change of 40 mm Hg; thus, when the PO2(alv) falls from100 to 60 mm Hg the blood saturation is reduced only by about eight percent. As the oxygen ten-

sion continues to fall, however, an additional reduction of 30 mm Hg results in a precipitous drop

in blood saturation to 58 percent. Thus, the characteristic shape of the dissociation curves ac-counts for the relatively mild effects of hypoxia at low altitude and the very serious impairment offunction at higher altitudes.

The oxygen carrying capacity of the blood hemoglobin is also very sensitive to changes in blood

pH (Bohr effect), as illustrated in Figure 1- 4B. At an oxygen tension of 60 mm Hg, for example,at pH 7.2, 7.4, and 7.6, the arterial oxygen saturation is observed to be 84, 89 and 94 percent,respectively. Carbon dioxide is the major determinant of blood pH. In venous blood PCO2 is

high; accordingly, the pH is low. In arterial blood, the PCO2 is less as a result of the diffusion ofcarbon dioxide into the alveoli. The arterial blood, therefore, has a higher pH and can carry moreoxygen at a given alveolar PO2 that would be possible without this change in pH. In the tissues,

the reverse conditions exists.

1 -16


Figure 1-4. A. Effect of CO2 on oxygen dissociation curve of whole blood (after Barcroft). B. Ef-

fect of acidity on oxygen dissociation curve of blood (after Peters & Van Slyke). C. Effect oftemperature on oxygen dissociation curve of blood (Carlson, 1956b).

Control of Respiration

The neural control of respiration is accomplished by neurons in the reticular formation of the

medulla. This rhythmic activity is modified by afferent impulses arising from receptors in various

parts of the body, by impulses originating in higher centers of the central nervous system, and byspecific local effects induced by changes in the chemical composition of the blood.

A major decrease in arterial PO2 causes slightly increased pulmonary ventilation. However, ifthe afferent fibers from the chemoreceptive areas are severed, respiration is depressed. Thus, the

1-17


direct effect of hypoxia on the respiratory center itself is depressive, but hypoxia will cause in-

creased pulmonary ventilation when the chemoreceptor mechanism is intact.

A minute increase of about 0.25 percent alveolar carbon dioxide will lead to a 100 percent in-crease in pulmonary ventilation rate. Conversely, lowering the alveolar PCO2 by voluntaryhyperventilation tends to produce apnea. From these observations, it may be deduced that con-trol of respiration appears to be governed primarily by the homeostasis of alveolar PCO2.

Oxygen lack is a rather ineffective stimulus for pulmonary ventilation. Ernsting (1965b) reportsthat no increase in pulmonary ventilation occurs with acute oxygen lack until the alveolar PO2 is

reduced to about 65 mm Hg, or at approximately 37,000 to 39,000 feet equivalent altitude,breathing 100 percent oxygen. Even a reduction alveolar oxygen to about 40 mm Hg (42,000 feetequivalent altitude) will only increase ventilation by about one third of its normal resting value.

The pattern of pulmonary ventilation occurring in hypoxia does not represent a simple reaction to

the reduced alveolar oxygen tension.

Hypoxia

Probably the most frequently encountered hazard in aviation medicine is hypoxia. Records ofearly balloon and aircraft flights describe tragedies resulting from hypoxia, since even these

primitive machines had a higher operational ceiling than the men aboard them.

Hypoxia was a serious aviation problem in both World Wars and remains a potential threat

even in today’s military aviation. Engineering solutions to the problem have been ingenious. Con-

siderable money has been expended on training of aviators and on procurement of equipment toprevent hypoxia. Yet, hypoxic incidents continue to occur, and the flight surgeon should be wellinformed concerning this problem.

There is a commonly encountered misconception among aviators that it is possible to learn all

of the early symptoms of hypoxia and then to take corrective measures once symptoms are noted.

This concept is appealing because it allows all action, both preventive and corrective, to bepostponed until the actual occurrence.

Unfortunately, the theory is both false and dangerous. One of the earliest effects of hypoxia is

impairment of judgment. Therefore, even if the early symptoms are noted, an aviator may

disregard them and often does, or he may take corrective action which is actually hazardous, such

as disconnecting himself from his only oxygen supply. Finally, at high altitudes, hypoxia may

cause unconsciousness as the first symptom.

1-18

Physiology of Fight

These factors must be kept in mind during a flight surgeon’s study of hypoxia, during the in-

doctrination and refresher training flights in the altitude chamber at an Aviation PhysiologyTraining Unit, and especially during the flight surgeon’s daily contact with aviators in the readyroom, sickbay, or clinic.

Despite improvements in oxygen delivery systems, more reliable cabin pressurization systems,and extensive physiology training, hypoxia still remains ever present in today’s military aviation.

Each year, approximately 8 to 10 physiological episodes of hypoxia are reported. The most com-

mon cause of the hypoxic incident is cabin or cockpit pressurization failure followed by defective

oxygen equipment. In these incidents, the pilot or copilot was able to recover the aircraft andavoid a major mishap or fatality. One can only conjecture how many mishaps and fatalities inmilitary aviation have occurred as the direct result of hypoxia. Since hypoxia episodes are still fre-quently encountered, and in all likelihood contribute to many major mishaps and fatalities, theflight surgeon and aviation physiologist should be well informed of every facet of the problem.

Types of Hypoxia

The amount and pressure of oxygen delivered to the tissues is determined by arterial oxygen

saturation, by the total oxygen-carrying capacity, and by the rate of delivery to the tissues.Hypoxia, defined as an insufficient supply of oxygen, can result from any one of these factors.Accordingly, the following classic types of hypoxia have been distinguished:

1. Hypoxic hypoxia results from an inadequate oxygenation of the arterial blood and iscaused by reduced oxygen partial pressure.

2. Anemic hypoxia results from the reduced oxygen- carrying capacity of the blood, whichmay be due to blood loss, any of the anemias, carbon monoxide poisoning, or by drugscausing methemogiobinemia.

3. Stagnant hypoxia is caused by a circulatory malfunction which results, for example, fromthe venous pooling encountered during acceleration maneuvers.

4. Histofoxic hypoxia results from an inability of the cells to utilize the oxygen providedwhen the normal oxidation processes have been poisoned such as by cyanide. There is nooxygen lack in the tissues, but rather an inability to use available oxygen, with the result

that the PO2 in the tissues may be higher than normal. Therefore, it is not true hypoxia bythe definition used here.

l-19


The most common type of hypoxia encountered in aviation is hypoxic hypoxia. This results

from the reduced oxygen partial pressure in the inspired air caused by the decrease in barometricpressure. Other types may also affect aircrewmen, such as anemic hypoxia as seen in carbon

monoxide poisoning and stagnant hypoxia resulting during various acceleration profiles.

Types of Onset of Hypoxia

The onset of hypoxia varies with the cause. During ascent to altitude without supplementaryoxygen equipment, the onset of hypoxia is as gradual as the rate of ascent. As soon as an inspira-tion is completed, the alveolar gases approach equilibrium with the inspired gases, and similarly,

the arterial gases reach a very rapid equilibrium with the alveolar gases, but the change in

barometric pressure is gradual between breaths.

In the event of contamination or dilution of oxygen in the mask with some amount of cabin air,due to either a leaky mask or faulty tubing, onset of hypoxia is intermittent. Moreover, the effectsare inconsistent because the amount of hypoxia developing varies from one breath to the next,depending on leakage rate, altitude, and body position (which may cause the aperture of a leak tobe temporarily closed, partially open, or completely open). This type of hypoxia onset is difficult

to trace because it is often difficult to validate that a hypoxic incident occurred, much less todetermine the cause.

In the case of a supply hose disconnect or other cause of exposure to ambient air, whetherknown or unknown, the onset of symptoms will be determined by the altitude during exposure. If

such a disconnect is immediately discovered, and if no decompression is involved, the aircrewmen

should hold his breath while attempting to reconnect, because the alveolar PO2 is higher than the

ambient PO2. Breathing in such circumstances will cause a washout of oxygen from the tissues.This must be avoided as long as possible.

When rapid decompression occurs, the volume and pressure of alveolar gases become markedlyhigher than those of the ambient atmosphere, and sudden expulsion of the alveolar gases occurs.

At the end of the resulting involuntary expiration, the normal reaction is to inhale, and at the end

of that inspiration, the alveolar PO2 is in equilibrium with the ambient air. The resulting effectswill depend upon the PO2 at the terminal decompression altitude.

Symptomatology

Many observations have been made on the subjective and objective symptoms of hypoxia. A

detailed analysis of progressive functional impairment indicates that the effects of hypoxia fall in-

1-20


to four stages. Table l-7 summarizes the stages of hypoxia in relation to the altitude of occur-rence, breathing air or breathing 100 percent oxygen, and the arterial oxygen saturation.

Table 1-7

Stages of Hypoxia

1. Indifferent Stage. There is no observed impairment. The only adverse effect is on dark

adaptation, emphasizing the need for oxygen use from the ground up during night flights.

2. Compensatory State. The physiological adjustments which occur in the respiratory and cir-

culatory systems are adequate to provide defense against the effects of hypoxia. Factors such asenvironmental stress or prolonged exercise can produce certain decompensations. In general, inthis stage there is an increase in pulse rate, respiratory minute volume, systolic blood pressure,and cardiac output. There is also an increase in fatigue, irritability, and headache, and a decreasein judgment. The individual has difficulty with simple tests requiring mental alertness ormoderate muscular coordination.

3. Disturbance Stage. In this stage, physiologic responses are inadequate to compensate for theoxygen deficiency, and hypoxia is evident. Subjective symptoms may include headache, fatigue,lassitude, somnolence, dizziness, “air-hunger“, and euphoria. At 20,000 feet, the period of

useful consciousness is 15 to 20 minutes. In some cases, there are no subjective symptomsnoticeable up to the time of unconsciousness. Objective findings include:

a. Special Senses. Peripheral and central vision are impaired and visual acuity is diminished.

There is weakness and incoordination of the extraocular muscles and reduced range of accom-

1-21


modation. Touch and pain sense are lost. Hearing is one of the last senses to be affected.

b. Mental Processes. The most striking symptoms of oxygen deprivation at these altitudes areclassed as psychological. These are the ones which make the problem of corrective action so dif-

ficult. Intellectual impairment occurs early, and the pilot has difficulty recognizing an emergency

situation unless he is widely experienced with hypoxia and has been very highly trained. Thinkingis slow; memory is faulty; and judgment is poor.

c. Personality Traits. In this state of mental disturbance, there may be a release of basic per-sonality traits and emotions. Euphoria, elation, moroseness, pugnaciousness, and gross overcon-

fidence may be manifest. The behavior may appear very similar to that noted in alcoholic intox-

ication.

d. Psychomotor Functions. Muscular coordination is reduced and the performance of fine ordelicate muscular movements may be impossible. As a result, there is poor handwriting, stammer-ing, and poor coordination in flying. Hyperventilation is noted and cyanosis occurs, mostnoticeable in the nail beds and lips.

4. Critical Stage. In this stage of acute hypoxia, there is almost complete mental and physical

incapacitation, resulting in rapid loss of consciousness, convulsions, and finally in failure ofrespiration and death.

An important factor in the sequence cited above is the gradual ascent to altitude where the in-dividual can come to equilibrium with the gaseous environment, and physiological adjustments

have sufficient time to come into play. This occurs in military aviation only in cases where the

aviator is unaware that his oxygen is disconnected or in cases where leaks occur in the oxygensystem, causing gradual dilution of the oxygen with cabin air.

Of greatest concern to a flight surgeon is hypoxia resulting from the sudden loss of cabinpressure in aircraft operating at very high altitudes. Under these conditions, a loss of pressuriza-tion or oxygen supply will cause exposure of the aviator to environmental conditions so stressful

that physiological compensation cannot occur before the onset of unconsciousness.

Time of Useful Consciousness

The time of useful consciousness is that period between an individual’s sudden deprivation ofoxygen at a given altitude and the onset of physical or mental impairment which prohibits his tak-ing rational action. It represents the time during which the individual can recognize his problem

1-22


and reestablish an oxygen supply, initiate a descent to lower altitude, or take other corrective ac-tion. Time of useful consciousness is also referred to as effective performance time (EPT).

The time of useful consciousness is primarily related to altitude, but it is also influenced by in-dividual tolerances, physical activity, the way in which the hypoxia is produced and the en-vironmental conditions prior to the exposure. Average times of useful consciousness at rest andwith moderate activity at various altitudes are shown in Table 1-8. The subjects were breathing

oxygen and produced the hypoxic environments by disconnecting their masks. If an individualbreathing air is suddenly decompressed, his time of useful consciousness is shorter than if he hadbeen breathing oxygen (Figure 1-5). The PO2 in his lungs drops immediately to a level dependent

only on the final altitude, rather than dropping gradually with each breath of air, dependent onlung volume, dilution of that volume, and altitude.

Table l-8

Time of Useful Consciousness

1-23

U.S. Naval Plight Surgeon’s Manual

Figure 1-5. Minimum and average duration of effective consciousness in subjects following rapid

decompression breathing air (lower curve) and O2 (upper curve) (Billings, 1973a; data fromBlockley & Hanifan, 1961).

Limit Altitudes and Altitude Equivalents

In considering hypoxia, some minimum limit must be set on the supply of oxygen considered

‘adequate’ for the purposes of military aviation. Ideally, one would select sea level conditions asthe limit and design and construct oxygen supply systems to maintain them, but this is not feasible

considering the altitudes at which Navy and Marine Corps aircraft are capable of operating.

In determining a limit altitude, one is actually specifying the maximum level of hypoxia whichis acceptable. The Navy NATOPS Manual, General Flight and Operating Instructions, OPNAVInstruction 3710.7 series, specifies the following limit altitudes for crew members aboard naval

aircraft: With one exception, all occupants aboard naval aircraft will use supplemental oxygen onflights in which the cabin altitude exceeds 10,000 feet.

Exception: When all occupants are equipped with oxygen, unpressurized aircraft may ascend toflight level 250 (25,000 feet). When minimum enroute altitudes or an ATC clearance requires

flight above 10,000 feet in an unpressurized aircraft, the pilot at the controls shall use oxygen.

1-24


When oxygen is not available to other occupants, flight between 10,000 and 13,000 feet shall notexceed three hours duration, and flight above 13,000 feet is prohibited.

Table 1-9 gives the oxygen requirements for pressurized aircraft flown above 10,000 feet, whencabin altitude is maintained at 10,000 feet or less. The quantity of oxygen aboard an aircraftbefore takeoff must be sufficient to accomplish the planned mission. In aircraft carrying

passengers, there must be an adequate quantity of oxygen to protect all occupants through nor-

mal descent to 10,000 feet.

Table 1-9

Oxygen Requirements for Pressurized Aircraft Other Than Jet Aircraft

1-25


If loss of pressurization occurs, a descent shall be made immediately to a flight level where

cabin altitude can be maintained at, or below, 25,000 feet, and oxygen shall be utilized by all oc-

cupants.

When it is observed or suspected that an occupant of any aircraft is suffering the effects of

decompression sickness, 100 percent oxygen will be started and the pilot shall immediately de-scend and land at the nearest civilian or military installation, and obtain qualified medicalassistance. The person affected may continue the flight only on the advice of a flight surgeon.

In tactical jet and tactical jet training aircraft, oxygen shall be used by all occupants from

takeoff to landing. Emergency bailout bottles, when provided, shall be connected prior to flight.

Respiratory Adjustments to Altitude

The critical PO2(alv) at which the average individual loses consciousness on short exposure to

altitude is 30 mm Hg. This corresponds to 23,000 to 25,000 feet on Curve A of Figure l-6. In thecomplete absence of respiratory adjustments to altitude, the same PO2(alv) would be en-countered at about 17,000 feet.

Applying similar considerations to 100 percent oxygen breathing altitudes, it is evident thathypoxia-induced hyperventilation, as reflected in the course of the PCO2(alv) on Curve D of

Figure 1-6, does improve the PO2(alv) measurably. Thus, the 30 mm Hg PO2(alv) in this case is at

47,000 feet (Curve C) with respiratory adjustment and 44,000 feet without it.

Comparisons can be made between different barometric pressures which produce the samealveolar PO2 when breathing air in one case and 100 percent oxygen in the other, in order to

establish “physiologically equivalent altitudes.” Actually, physiological states cannot be com-pared solely on the basis of PO2(alv). PCO2(alv) and ventilation must be considered also, since achange in one will cause change in the others until a steady state is reached.

l -26


Figure l-6. The partial pressures of respiratory gases when breathing air (A, oxygen; B, carbondioxide) and using oxygen equipment (C, oxygen; D, carbon dioxide). The interrupted lines

represent the theoretical course in the absence of the respiratory response to hypoxia at altitude(Boothby, Lovelace, Benson & Strehler, 1954).

The time necessary to reach a steady state at various altitudes is given in Figure 1-7. Note thateven at the relatively low altitude of 18,000 feet, a steady state is reached only after an hour ofrespiratory adjustment. For practical purposes, the PO2(alv) may be used without considering

respiratory adjustment in establishing physiologically equivalent altitudes.

Ten thousand feet during daylight is specified as the limit above which, in non-pressurized air-craft, crew members must use oxygen. The PO2(alv) at 10,000 feet, breathing air, is approximate-

ly 61 mm Hg, which produces the maximum acceptable degree of hypoxia which Navy and

Marine Corps aircrewmen are allowed to undergo. As a consequence, all oxygen equipment andbarometric controls are designed to maintain the user at this physiological equivalent or below.

1-27


Figure 1-7. The respiratory exchange ratio in the course of exposures to l0,000, 15,000, 18,000

and 25,000 feet, indicating the duration of the “unsteady state” (Boothby, Lovelace, Benson, &Strehler, 1954).

Having arrived at the allowable lower limit of PO2(alv), various equivalent altitudes yielding

the same PO2(alv) can be compared. In breathing oxygen not under pressure, Table l-10 shows aPO2(alv) of 61 mm Hg at 39,500 feet, which is, therefore, the upper limit for flying without

positive pressure breathing. Similarly, other limiting altitudes are noted.

A question may arise as to why 10,000 feet while breathing air, or a PO2(alv) of about 60 mmHg, was selected as the upper limit for flight without oxygen. Reference to Table l-6 shows that10,000 feet is the upper limit for the indifferent stage of hypoxia. Even more important, reference

to the oxyhemoglobin saturation curve shows that ascent to 10,000 feet causes a decrease of only

about seven percent in the oxyhemoglobin saturation, since at 10,000 feet the hemoglobin is still90 percent saturated. However, rather small increases in altitude thereafter cause a rather marked

1-28


Table l-10

Limiting Altitude for Respiratory Functioning

steepening of the slope of the curve. Certainly a 2,000 to 3,000 foot difference would not matter

much, but anything over that becomes unacceptable; hence, the NATOPS limitation to 13,000feet for not over three hours for certain types of flights.

1 -29


The theoretical considerations just discussed set limits which are useful in making predictionsand calculations. In military operations, however, many variable factors must be taken into ac-count. If the oxygen mask suspension is not tightly adjusted, or if the mask is improperly fitted to

the aviator, a lower PO2(alv) will be measured in the individual using that equipment than wouldbe predicted, due to dilution of the inspired oxygen with cabin air. There are other factors which

could also account for considerable variation in the absolute PO2 delivered to the trachea at the

same altitude using the same equipment at the same settings, but on different days or even dif-ferent flights.

Individual variations in diffusion rates for the alveolar membrane, or in the amount of cir-culating hemoglobin, or in several other physiological variables, could also result in a lowerarterial PO2 than expected from the same PO2(alv). The significance is that the range of variabili-

ty both in supply and among individuals must be compensated for by the supply of oxygen. The

mechanical means will be discussed later, but one example of the built-in safety factors in oxygenequipment is given here.

From calculations of PO2(alv) as noted in Table 1-10, 33,700 feet is the altitude at which an in-

dividual breathing 100 percent oxygen has the same PO2(alv) as an individual breathing air at sealevel. If no safety factor were included, the aneroid of the diluter-demand oxygen regulator would

be set so that the regulator would deliver 100 percent oxygen at that altitude. Oxygen would be

wasted if the regulator were set to deliver 100 percent at any lower altitude. (The reason for at-tempting to conserve oxygen is that oxygen quantity, like fuel quantity, is a limiting factor on air-craft range.)

In actuality depending upon the diluter-demand regulator utilized, 100 percent oxygen is

delivered between 20,000 to 32,000 feet rather than at 33,700 feet. Such safety factors are built in-

to almost all Navy life support equipment, not only to anticipate the wide variation in human

response, but also to guard against some slight misuse or maladjustment of the equipment.

The theoretical upper limit of altitude which can be endured by the unprotected body is thepoint at which the ambient pressure is equal to or lower than the vapor pressure of water at abody temperature 98.6° F. Above that limit, much of the water in the body would vaporize.

Theoretically, this would occur at 63,000 feet with a barometric pressure of 47 mm Hg. Actually

this "critical" altitude must be modified upward since the water in the body is contained in the

pressure vessels of cells, intravascular spaces, etc. The only situation in which the body watermight vaporize is one in which an aviator who is flying at or above this altitude limit, with the

cabin pressurized to a much lower altitude, experiences a rapid decompression to ambientpressure.

1-30


This upper limit has been tested experimentally and appears to be rather on the low side of theactual figure.

In experiments on the unprotected human hand (Figure 1-8), it was found that a pressure below

that equal to water vapor pressure at skin temperature was required to cause vaporization of bodywater. The discrepancy may have been due to the forces exerted by connective tissues within thehand and the elastic nature of the skin covering.

Figure 1-8. Water vapor in tissue at extreme altitudes (Billings & Roth, 1964).

Appearance of water vapor occurred suddenly and manifested itself by marked swelling of the

hand after a variable time at altitude. After appearance of swelling, the pressure in the altitude

chamber was quickly raised; the hand was examined periodically. The upper point (o) representsthe first point at which swelling was no longer visible to the eye.

If chamber pressure was again lowered slightly, swelling again appeared, indicating the con-tinued presence of bubble nuclei in the hand tissues. This suggests that once water vapor bubbles

1-31


appear, oxygen and carbon dioxide diffuse into the bubbles, which become transformed intobubbles of gas saturated with water vapor.

For the Navy and Marine Corps aviator, the NATOPS Manual, OPNAVINST 3710.7 series

limits flights in pressurized aircraft flown by aviators not utilizing full pressure suits to 50,000feet.

Hyperventilation

Among the perils that test the prudence and stamina of a pilot and is closely associated withhypoxia, is a breathing disorder called hyperventilation. Although unrelated in cause, the symp-toms of hyperventilation and hypoxia are similar and often result in confusion and inappropriatetreatment.

Definition of Hyperventilation

Hyperventilation is defined as excessive rate or depth of breathing. The increase in ventilationleads to a lowering of alveolar carbon dioxide tension, a condition referred to as hypocapnia. Inaddition, the acid-base balance of the blood becomes more alkaline, a condition referred to as arespiratory alkalosis.

Causes of Hyperventilation

Among the causes that can lead to hyperventilation are hypoxia, pressure breathing,psychological stress, and pharamocological stimuli.

Hypoxia With the onset of hypoxia above 10,000 feet, oxygen tension in the lungs and arterial

blood is reduced. This reduced arterial PO2 reflexively stimulates the respiratory center via the

aortic and carotid peripheral chemoreceptors, causing increased breathing.

Pressure Breathing. There is a tendency to over breathe during positive pressure breathing.Positive pressure which is used to prevent hypoxia, creates a reversal of the normal respiratory cy-cle of inhalation and exhalation. Under positive pressure breathing, the aviator is not actively in-

volved in inhalation as in the normal respiratory cycle. Instead of the aviator inhaling oxygen into

the lungs, oxygen, under pressure, is forced into the lungs. During exhalation under positive

pressure breathing, the aviator must breathe out against pressure. The force that the individual

must exert in exhaling results in an increased rate and depth of breathing.

1-32


Psychological Stress. The human psyche can also override the normal respiratory controls.Fear, anxiety, stress or tension, resulting from emotion or physical discomfort, will sometimescause an individual to override the normal reflex control of breathing. This cause is most fre-quently encountered during initial low pressure chamber flights and early inflight training, and isprobably the most common cause in all types of flying.

Pharmacological Stimuli. Pharmacological stimuli to hyperventilation only become importantwhen aircrew who are taking drugs continue to fly. The major groups of drugs that causehyperventilation are salicylates, female sex hormones, catecholamines and analeptics.

Effects of Hyperventilation

The two primary results of hyperventilation are hypocapnia and alkalosis. The hypocapnia and

alkalosis have an effect on the respiratory, cardiovascular and central nervous systems.

Respiratory System. The effect of hyperventilation on the respiratory system is primarily on theblood buffer system. Seventy percent of the carbon dioxide present in the blood is carried as abicarbonate ion. The overall reaction for bicarbonate formation occurs as follows:

The major influence determining the direction in which the above reaction proceeds is the con-

centration, or partial pressure of carbon dioxide. When the carbon dioxide levels in the blood in-crease, the reaction proceeds to the right, toward the formation of greater hydrogen and bicar-bonate ions. When the carbon dioxide level decreases, the reaction reverses toward the formationof carbon dioxide and water. When an individual hyperventilates, the excessive elimination of

carbon dioxide causes a reduction in hydrogen ion concentration that is too rapid for the bloodbuffer system to replace. The pH is elevated and a respiratory alkalosis ensues.

Cardiovascular System. It is generally agreed that hyperventilation causes tachycardia, increas-ed cardiac output and reduced systemic vascular resistance and mean arterial blood pressure.

Hyperventilation also causes vasoconstriction of cerebral blood vessels, vasodilation of systemicblood vessels and reduced coronary blood flow resulting in lowered myocardial oxygen tension.The combined effects of systemic vasodilation and cerebral vasoconstriction cause a restriction in

blood flow to the brain. The primary cardiovascular effect is on the oxyhemoglobin dissociation

nerve. Hyperventilation shifts the oxyhemoglobin curve upward and to the left, called the Bohreffect. This shift increases the capacity of blood to onload oxygen on the lung level but restricts

1-33


offloading at the tissue level. The combined effect of restricted blood flow and increased oxygen

binding results in stagnant hypoxia at the brain which leads to unconsciousness.

Central Nervous System. Hyperventilation and the resulting elevated pH cause an increased

sensitivity and irritability of neuromuscular tissue. This increase is manifested by superficial tingl-ing and numbness of the extremities and mouth, and muscular spasm and tetany. The tinglingusually precedes muscular spasm and tetany. The hands and feet may exhibit carpopedal spasm, a

fixation of the hand wherein the fingers are flexed toward the wrist or a marked plantar flexion of

the ankle. Muscle spasm usually occurs when the arterial carbon dioxide tension has been reducedto 15 to 20 mm Hg. In more severe hypocapnia, with an arterial carbon dioxide tension less than

15 mm Hg, the whole body becomes stiff (tetany) due to contraction of skeletal muscle. Figure

1-9 summarizes the effects of hyperventilation.

Figure l-9. Effects of hyperventilation.

l-34


Signs and Symptoms of Hyperventilation

The signs and symptoms of hyperventilation are not easily differentiated from and can easily beconfused with those of hypoxic hypoxia.

Objective Signs. The objective signs of hyperventilation most often observed in another in-dividual are:

1. Increase rate and depth of breathing.

2. Muscle twitching and tightness.3. Paleness.4. Cold clammy skin.

5. Muscle spasms.

6. Rigidity.7. Unconsciousness.

Subjective Symptoms. The subjective symptoms, those perceived by the individual include:

1. Dizziness.

2. Light headedness.3. Tingling.4. Numbness.5. Muscular incoordination.6. Visual disturbance.

Similarity to Hypoxia

While the etiology of hypoxia and hyperventilation are different, the symptoms are quitesimilar making it difficult to differentiate between the two. There are, however, a fewdistinguishing differences in these two syndromes. In hyperventilation, the onset is gradual, withthe presence of pale, cold, clammy skin and the development of muscle spasm and tetany. Inhypoxia, the onset of symptoms is usually rapid (altitude-dependent), with the development of

flaccid muscles and cyanosis.

Treatment of Hyperventilation

Since hypoxia and hyperventilation are so similar and both can quickly incapacitate, the recom-mended treatment is aimed at correcting both problems simultaneously. There are five steps fortreatment:

1-35


1. Go to 100 percent oxygen if not already on it.2. Check oxygen equipment to ensure proper functioning.

3. Control breathing - reduce the rate and depth.4. Descend below 10,000 feet where hypoxia is an unlikely problem.5. Communicate problem.

Positive Pressure Breathing

The requirement for positive pressure breathing in naval aviation is predicated on the degree of

hypoxia acceptable for safe mission performance. Safe mission performance is based on a

minimal alveolar partial pressure of oxygen of 60 mm Hg. This alveolar partial pressure of oxygenis reached at approximately 39,000 feet breathing 100 percent oxygen. To maintain the minimum

alveolar partial pressure of oxygen above 39,000 feet, positive pressure must be applied to the

breathing oxygen.

Positive pressure breathing in operational aircraft is an indication of an emergency conditionwhich occurs when cabin pressurization is lost at or above 35,000 feet, In the event of cabinpressurization failure at altitudes above 35,000 feet, pressure breathing is employed to maintainconsciousness and physical function so that a rapid controlled descent to lower altitudes may be

accomplished. As long as the cabin pressurization system is functioning normally, the aviatorshould not experience positive pressure breathing.

Kinds of Positive Pressure Breathing

Simply stated, positive pressure breathing is the delivery of a gas to the respiratory tract at apressure greater than ambient. There are two kinds of positive pressure breathing: intermittent

positive pressure breathing and continuous positive pressure breathing.

Intermittent Positive Pressure Breathing (IPPB). IPPB provides pressure behind the breathing

gas on inspiration, but during expiration the pressure is removed. The mean mask pressure is ap-proximately one third of the highest pressure applied during the inspiratory phase.

Continuous Positive Pressure Breathing (CPPB). CPPB provides pressure behind thebreathing gas throughout the respiratory cycle. Assuming a good mask fit without leakage, themean mask pressure is nearly equivalent to the positive pressure delivered by the regulator, and

the alveolar gas pressure is correspondingly raised. The highest mean mask pressure of oxygen of-

fers the best physiological protection against hypoxic hypoxia. Since this is obtained with CPPBbreathing, this system is utilized in Naval aviation.

1-36


Respiratory Effects of Positive Pressure Breathing

Distention of Lungs and Chest. The stress on the walls of the lungs normally depends upon

their degree of inflation, the support of the walls of the thoracic cavity and the maximum pressurewhich can be exerted and held in the lungs by active contraction of the expiratory muscles.Pressure breathing tends to distend the chest and lungs. In a relaxed individual, when nomuscular effort is made, the lungs are fully distended by a pressure of 20 mm Hg. If the lungs areunsupported by the chest wall (i.e., open thorax) they will rupture when the intrapulmonary

pressures exceeds 40-50 mm Hg. When, however, the chest wall is intact, intrapulmonary

pressures up to 80 to 100 mm Hg can be tolerated without damage. At intrapulmonary pressures

between 80 to 100 mm Hg, parenchymal lung damage secondary to overexpansion may occur ifthe expiratory muscles are relaxed. While overdistention of the lung is possible, lung rupture isnot probable. The greatest pressure output of current naval regulators is 30 mm Hg, well below

the threshold of lung damage even in an open chest.

Pulmonary Ventilation. In most subjects, pressure breathing causes an increase in minute ven-

tilation. The increase is due to both an increase in tidal volume and frequency of breathing. There

is a wide variation in pulmonary ventilation response which depends to a great extent on in-dividual experience with positive pressure breathing. Pressure breathing at 30 mm Hg causes amean increase in the respiratory minute volume of 50 percent over the resting valve. Some in-

dividuals double their minute volume at 30 mm Hg while others hardly respond.

Intrapleural Pressure. The increase in intrapleural pressure which occurs during positive

pressure is important since it determines the magnitude of insult on the cardiovascular system.

The increase in the intrapleural pressure is a function of the applied positive pressure and thedegree of lung distention. If there is no increase in lung volume, the intrapleural pressure will

equal the applied positive pressure. If lung distension occurs, the intrapleural pressure will be lessthan the breathing pressure by an amount equal to the pressure produced by the elastic recoil ofthe distended lung. The elastic recoil pressure of the lung is approximate 4 mm Hg per liter oflung distension. If for example, the lung volume is increased by 4 liters, the rise in intrapleural

pressure will be approximately 16 mm Hg less than the applied positive pressure.

Breathing Effort. In continuous positive pressure breathing the normal breathing cycle of an

active inspiration and passive expiration is reversed to a passive inspiration and an active expira-tion. This reversal in cycle makes the act of breathing more difficult and increases the work ofbreathing. Experienced subjects can breathe for short periods at pressures up to about 50 mm Hg,

whereas those unaccustomed to this maneuver cannot tolerate breathing pressures greater than 30

mm Hg.

1-37


Circulatory Effects of Positive Pressure Breathing. The circulatory disturbances produced bypositive pressure breathing depend upon the magnitude and duration of the applied pressure.Positive pressure breathing increases intrapulmonary pressure which in turn results in an increasein intrapleural pressure. It is the rise in intrapleural pressure rather than the increase in in-

trapulmonary pressure that determines the stress applied to the circulatory system. The heart and

intrathoracic vessels are normally subjected to intrapleural pressure. The diastolic pressure withinthese vessels will be raised at the beginning of positive pressure by an amount equal to the rise in

intrapleural pressure.

Venous Pooling. At the start of pressure breathing the increase in intrapleural pressure istransmitted to the right atrium and large intrathoracic veins. Since the pressure in the ex-

trathoracic vessels is normally low, this increase in central venous pressure seriously impedes theflow of blood from the systemic veins to the heart and venous outflow from the limbs completely

ceases.

Although venous outflow from the limbs ceases with the onset of positive pressure breathing,arterial inflow continues. Blood as a result, collects in and distends the venules and veins of the

peripheral vascular bed until peripheral pressure exceeds right atria1 pressure. At that pointvenous return is restored from the limbs thereby increasing the systemic venous return to theheart. This initial phase of reduction of venous return to the heart lasts about 10 to 20 seconds.

Reduction in Circulating Blood Volume. Effective blood volume, that volume of blood

available for circulation, is reduced during positive pressure breathing by two factors:

1. Initial pooling of blood (described above).

2. Passage of fluid from the capillaries into the tissue.

The rate at which fluid leaves the capillaries depend on the rise in capillary pressure which is

closely related to the increase in venous pressure. Pressure breathing for 10 minutes at 30 mm Hghas resulted in a loss of 250 ml of fluid while pressure breathing for 5 minutes at 100 mm Hg hasresulted in a loss of 500 ml of fluid into the tissue. The total reduction in effective blood volumewhich occurs during pressure breathing results from the combined effects of initial pooling of

blood and the passage of fluid from the circulation into the tissue. During pressure breathing at

30 mm Hg for 10 minutes total reduction is of the order of 450 ml. Pressure breathing at 100 mm

Hg for 5 minutes reduces the effective blood volume in the order of 950 ml.

Reduced Cardiac Output. The reduction in effective blood volume due to pooling of blood and

increase in extravascular fluid results in a reduced cardiac output. Pressure breathing at 30 mm

1-38


Hg without trunk counterpressure reduces cardiac output some 30 percent. If counterpressure isapplied, 30 mm Hg pressure breathing reduces cardiac output by 15 to 20 percent.

Advantages of a Positive Pressure Breathing

1. The equipment is inexpensive, reliable, instantly available, and requires comparatively lit-

tle maintenance.

2. With a small amount of training, a definite increase in service ceiling can be obtained.

Disadvantages of Positive Pressure Breathing.

1. The service ceiling increase is small (about 5,000 feet) and limited.

2. The limitations are those caused by possible injury to the aviator.

3. Pressure breathing is opposite to the normal breathing pattern in that inhalation is passiveand exhalation active, thus requiring training and familiarization.

4. The process of pressure breathing is fatiguing.

5. Communications are much more difficult during pressure breathing.

6. Hyperventilation with resulting respiratory hypocapnia is very common even in moderate-ly experienced aviators.

Effectiveness of Positive Pressure

In view of the major side effects which include decreased venous return, decrease cardiac out-

put, increase arterial blood pressure, distention of extra thoracic veins, tachycardia, possible rup-ture of alveoli and possible snycope, 15 mm Hg represents a practical maximum for sustainedpositive pressure breathing. Since roughly 3 mm Hg pressure increase is required for each 1000

feet gain in altitude above 40,000 feet, the 15 mm Hg practical maximum raises the physiologicalaltitude ceiling only from 40,000 to 45,000 feet. This is not really a significant rise in terms ofaltitude capabilities of current and future operational aircraft. The emergency ceiling of pressure

breathing is 50,000 feet. At this altitude the pressure delivered is approximately 33 mm Hg. In

sudden decompression to 50,000 feet, positive pressure breathing can be utilized for a brief periodof time to sustain useful consciousness and permit a rapid descent to a lower altitude. Theminimum and maximum pressures delivered at various altitudes are summarized in Table 1-11.

1-39


Table 1-11

Positive Pressure Loading at 10 LPM Ambient Flow

Bailout Oxygen Supply

All tactical jet aircraft have an emergency oxygen supply in a high pressure oxygen cylinder.The cylinder is contained in the rigid seat survival kit of the ejection seat. For each type of aircraft

seat the cylinder capacity varies. In the F-14 the approximate oxygen supply time is 20 minutes

while in the F/A-18 it is 10 minutes. The emergency oxygen supply is automatically actuated dur-ing the ejection sequence.

Time to Ground. An emergency oxygen supply is necessary for use during the time required fordescent by free fall from high altitudes, or the even longer times when the parachute is openedprematurely. Table 1-12 shows that from 40,000 feet, time of useful consciousness is 18 seconds,

while time to free fall to 14,000 feet is 90 seconds, and time to descent to 14,000 feet is 900

seconds (or 15 minutes), with the 28 to 30 foot parachute open. Obviously, some provision mustbe made to keep the pilot alive during such a parachute descent. Barometrically actuatedparachute openers allow an aviator to free fall in the unconscious condition and survive, but ac-

cidental parachute deployment at high altitude would cause certain death or at least un-consciousness from hypoxia if emergency oxygen could not be supplied. Note that in Figure 1-10

the time to free fall from 28,000 feet to 14,000 feet is the same as the useful consciousness time at

28,000 feet. For rough approximations, therefore, 28,000 feet is the highest altitude from which

1-40


free fall can be accomplished while breathing ambient air and retaining consciousness. Actually,the time of useful consciousness increases as the subject falls, but this may be considered a safety

factor.

Table 1-12

Period of Useful Consciousness in High Altitude Bailout

1-41


Figure 1-10. Descent to safe breathing altitude (Carlyle, 1963).

Cabin Pressurization

The physiological zone which extends from sea level to 10,000 feet, encompasses the pressurearea to which man is well adapted. Although middle ear or sinus problems may be experienced

during descent or ascent in this zone, most physiological problems occur outside this zone if

suitable protective equipment is not utilized. In general, the most effective way of preventing

physiological problems from occurring is to provide cabin pressurization so that occupants are

never exposed to pressure outside the physiological zone. In these instances when ascent abovethe physiological zone is required, protective oxygen equipment and pressure garments must beprovided.

1-42


Methods of Maintaining Cabin Pressure

The higher the differential pressure required between cabin pressure and ambient pressure, the

greater the capacity of the pressurization system, and the stronger and heavier the fuselage con-struction; There are two methods of maintaining cabin pressure above ambient.

1. Sealed Cabins. At very high altitudes, a point is reached where the ambient air becomes so

thin that it is impossible for the compressor to scoop up enough air for compression.When this occurs the compressor stalls, and the pressurization fails. At approximately

80,000 feet ambient altitude, cabin pressurization cannot be accomplished via the conven-

tional method because of the “rarified” atmosphere. At this point, sealed cabins must beused to maintain an adequate environment. Pressurized gas is carried within the vehicleand the used gas recycled. Since this is a closed system, the environmental gas must be

continually purified and recirculated to conserve the supply (Figure 1-11). This system is

utilized at extremely high altitudes and in the vacuum of space.

Figure 1-11. Schematic of sealed cabin.

2. Conventional Method. The conventional method for increasing the pressure in aircraft

cabins is to use ambient air as the source of gas, forcing it into the cabin by means of a

1-43


compressor. Cabin pressures and ventilation can be controlled by varying the amount ofair forced into the cabin and the amount allowed to escape through adjustable outflowvalves (Figure 1-12).

Figures 1-12. Schematic of pressurized cabin.

The conventional method for cabin pressurization utilizes two types of pressurization

schedules. These are the isobaric and the isobaric- differential.

a. Isobaric System. Isobaric Control refers to the condition where the cabin altitude

is maintained at a constant altitude or pressure as the ambient pressure decreases(Figure 1-13). This type of pressurization system is found in most cargo andpassenger carrying aircraft. Military air transport aircraft (e.g., T-39, C-131,C-9, T-44, P-3) typically maintain a cabin pressure approximately equivalent to

8000 feet of altitude through the ceiling of the aircraft.

b. Isobaric-Differential System. Pressurization of aircraft cabins represents an ex-

cellent example of engineering tradeoff. A high differential requires an aircraft

structure which is physically stronger and therefore heavier than that requiredfor a lower differential. The increased weight in turn, decreases the payload ofthe aircraft. Pressurization requires an expenditure of energy; therefore, the

larger the differential the greater the power required to provide the desiredpressure and less power available for aircraft manuverability. Also, the higher

1-44


Figure 1-13. Isobaric pressure schedule.

the pressure differential, the greater the possibility of a rapid decompression.Tactical jet aircraft are equipped with an isobaric- differential pressurization

system. This pressurization system senses both cabin and ambient pressure andmaintains the cabin pressure on the basis of a fixed pressure differential of 5 psi.Figure 1-14 shows a typical isobaric-differential pressurization schedule found in

Navy tactical jet aircraft. As the aircraft climbs, the aircraft is unpressurized to

an altitude of 8,000 feet. From 8,000 feet to approximately 23,000 feet, cabinpressure remains at 8,000 feet (isobaric range). From 23,000 feet up to the ceiling

1-45


of the aircraft, the cabin pressure is maintained at a pressure differential of 5 psi.

For example, if an aircraft is flying at an indicated ambient altitude of 40,000feet where the pressure is 2.72 psi outside the aircraft, and the pressurization

system is in normal operation, the effective cabin altitude would be 7.72 psi or

approximately 16,500 feet.

Figure 1-14. F-14A aircraft cabin pressure schedule.

Advantages of Pressurized Cabins

Reducing the probability of hypoxia and decompression sickness are perhaps the two most im-

portant advantages of the pressurized cabin. Other advantages of cabin pressurization include:

1. Reduces the need for supplemental oxygen except in tactical jet aircraft where it is re-

quired from takeoff to landing.

2. Gastrointestinal trapped gas pains are reduced.

3. Cabin temperature, humidity and ventilation can be controlled within desired comfort

levels.

1-46


4. In large aircraft, the crew and passengers can move about freely in a comfortable environ-ment unencumbered by oxygen masks or other life support equipment.

5. Prolonged passenger flights, air evacuation, and troop movements can be accomplishedwith a minimum of fatigue and discomfort.

6. Protection against pain in the middle ear and sinuses can be provided by permitting thepressure in the cabin to rise slowly in a controlled manner during descent from high

altitude to ground level.

Disadvantages of Pressurized Cabins

The penalties for the above mentioned advantages are the following disadvantages:

1. Increased structural weight and strength of the pressurized area to maintain structural in-

tegrity.

2. Additional equipment and power requirements to support the pressurization, ventilation

and air conditioning systems.

3. Maximum performance and payload capacity of the aircraft is reduced because of addedweight.

4. Additional maintenance and upkeep is needed.

5. Possible contamination of the cabin air from smoke, fumes, carbon monoxide, carbon

dioxide and odors.

6. Should a rapid decompression occur, the occupants of the aircraft are exposed to the

dangers of hypoxia, decompression sickness, gastrointestinal gas expansion and

hypothermia. In addition, the cyclonic winds create the possibility of personnel being lostthrough the opening.

Rapid Decompression

Aircrew members are faced with many hazardous factors when performing duties involving fly-

ing. Decompression at altitude is one of those factors that can cause significant physiological pro-blems. Decompressions are categorized as either “slow” or “rapid”. A slow decompression can

1-47


occur when a leak develops in a pressure seal. This type of decompression is dangerous because ofthe possible insidious effect of hypoxia. Rapid decompressions are considered more dangerous.

They can occur as a result of a perforation of the cockpit or cabin wall or unintentional loss of the

canopy or hatch.

Factors Controlling the Rate and Time of Decompression

The principal factors that govern the total time of decompression include the cabin volume,

size of the opening, the pressure ratio, and the pressure differential.

Volume of the Pressurized Cabin. The decompression time within a larger cabin area will be

considerably slower than that of a cabin with less area.

Size of the Opening. The proportionality of cabin volume and cross sectional area of the open-ing dictates the decompression rate and time.

Pressure Ratio. Variables involved in determining the time of decompression are the pressurewithin the cabin and the outside ambient pressure. If the pressure ratio is increased, then it can be

presumed